Nevertheless, in vitro experiments with human neutrophils demonstrated that treatment with C5a or the acute phase-protein C-reactive-protein (CRP)—both of which are significantly enhanced in plasma during septic shock—resulted in an almost complete loss of C5aR1 on neutrophils, and significantly increased numbers of MVs carrying C5aR1 on their surface leading to an acquired dysfunction of neutrophils (10). This evidence concerns the gene CRP and Shock.